The cause of the elevated peripheral resistance in hypertension remains unclear. Toxemia of pregnancy affords a model of reversible hypertension containing many features of significance in essential hypertension; i.e., aberrations in plasma renin and angiotensin sensitivity, possible changes in prostaglandin E synthesis, loss of fine volume control as evidenced by salt retention. An understanding of this common disease would not only reduce maternal mortality and morbidity but may also give insight into mechanisms of hypertension in other conditions. Since the kidney and uterus both synthesize renin and PGE, understanding the factors controlling uterine PGE synthesis may aid in defining a role of PGE in blood pressure control. Renal medullary PGE could act as a modulator of peripheral resistance by antagonism to the renal and peripheral vasoconstrictor effect of angiotensin and it may exert an effect upon extracellular fluid volume by altering collecting tubule sodium and water absorption. Since blood vessels synthesis PGE another role could be controlling effective blood volume by altering venous capacitance which is an afferent limb to the kidney's control of sodium absorption.